Biomedical subjects

Thomas C Glenn

Publications and source records attributed to Thomas C Glenn.

16 recordsLinked to original sources

PubMed2006

Nonlinear analysis of cerebral hemodynamic and intracranial pressure signals for characterization of autoregulation.

The objective of this study was to determine whether or not the underlying physiological systems that generates spontaneous arterial blood pressure (ABP), cerebral blood flow velocity (CBFV), and intracranial pressure signals could be adequately approximated as a linear stochastic process. Furthermore, a new measure (C) capable of capturing the degree of nonlinear dependency between two ABP and CBFV signals (including a time-varying situation) was proposed for quantifying the degree of cerebral blood flow autoregulation. A surrogate data test of fifteen ABP, CBFV, and intracranial pressure (ICP) segments was conducted for detecting whether there exists a statistically significant deviation from the null hypothesis of linear signals. The extension of the established block computation method of C measure to an adaptive one was achieved. This new algorithm was then applied to study the C evolution using brain injury patients data from a hyperventilation study and two propofol studies. Nonlinearity has not been detected for all the fifteen recordings, neither has nonlinear dependency between CBFV and ABP. However, their presences in some of the signal segments justified the adoption of a nonlinear measure of dependency capable of characterizing both linear and nonlinear correlations for inferring autoregulation status. C measure started to decrease with the introduction of hypocapnia state indicating that hyperventilation may reduce the dependency of CBFV on ABP fluctuations. On the other hand, complex patterns of C measure evolution were observed among 14 cases of propofol data indicating a nontrivial effect of propofol on the dependency of CBFV on ABP.

Adaptation, Physiological↗

PubMed2005

Comparative overview of brain perfusion imaging techniques.

BACKGROUND AND PURPOSE: Numerous imaging techniques have been developed and applied to evaluate brain hemodynamics. Among these are positron emission tomography, single photon emission computed tomography, Xenon-enhanced computed tomography, dynamic perfusion computed tomography, MRI dynamic susceptibility contrast, arterial spin labeling, and Doppler ultrasound. These techniques give similar information about brain hemodynamics in the form of parameters such as cerebral blood flow or cerebral blood volume. All of them are used to characterize the same types of pathological conditions. However, each technique has its own advantages and drawbacks. SUMMARY OF REVIEW: This article addresses the main imaging techniques dedicated to brain hemodynamics. It represents a comparative overview established by consensus among specialists of the various techniques. CONCLUSIONS: For clinicians, this article should offer a clearer picture of the pros and cons of currently available brain perfusion imaging techniques and assist them in choosing the proper method for every specific clinical setting.

Aged↗

PubMed2005

Metabolic crisis without brain ischemia is common after traumatic brain injury: a combined microdialysis and positron emission tomography study.

Brain trauma is accompanied by regional alterations of brain metabolism, reduction in metabolic rates and possible energy crisis. We hypothesize that microdialysis markers of energy crisis are present during the critical period of intensive care despite the absence of brain ischemia. In all, 19 brain injury patients (mean GCS 6) underwent combined positron emission tomography (PET) for metabolism of glucose (CMRglu) and oxygen (CMRO(2)) and cerebral microdialysis (MD) at a mean time of 36 h after injury. Microdialysis values were compared with the regional mean PET values adjacent to the probe. Longitudinal MD data revealed a 25% incidence rate of metabolic crisis (elevated lactate/pyruvate ratio (LPR) > 40) but only a 2.4% incidence rate of ischemia. Positron emission tomography imaging revealed a 1% incidence of ischemia across all voxels as measured by oxygen extraction fraction (OEF) and cerebral venous oxygen content (CvO(2)). In the region of the MD probe, PET imaging revealed ischemia in a single patient despite increased LPR in other patients. Lactate/pyruvate ratio correlated negatively with CMRO(2) (P < 0.001), but not with OEF or CvO(2). Traumatic brain injury leads to a state of persistent metabolic crisis as reflected by abnormal cerebral microdialysis LPR that is not related to ischemia.

Acute Disease↗

PubMed2005

Monitoring of cerebral blood flow and metabolism in traumatic brain injury.

The aim of the present study was to investigate the course of cerebral blood flow (CBF) and metabolism in traumatic brain injury (TBI) patients and to specifically characterize the changes in lactate and glucose indices in the acute post-traumatic period with regard to neurological condition and functional outcome. For this purpose, 55 consecutive TBI patients (mean age 37 +/- 17 years, mean GCS 6.8 +/- 3.2) were prospectively and daily evaluated. Global CBF, cerebral metabolic rates of oxygen (CMRO2), glucose (CMRGlc), and lactate (CMRLct) were calculated using arterial jugular differences. In all patients, CBF was moderately decreased during the first 24 h in comparison with normal subjects although this relative oligemia was more pronounced in patients with poor outcome (p = 0.0007). Both CMRO2 and CMRGlc were significantly depressed and correlated to outcome (p < 0.0001, p = 0.0088). CMRLct analysis revealed positive values (lactate uptake) during the first 48 h, especially in patients with favorable outcome. Both CMRO2 and CMRLct correlated with GCS (p = 0.0001, p = 0.0205). CMRLct levels showed an opposite correlation with CBF in patients with favorable and poor outcome. In the former group, correlation analysis exhibited a negative slope with evidence for increasing lactate uptake associated with lower CBF values (r = -0.1940, p = 0.0242). On the contrary, in patients with adverse outcome, CMRLct values demonstrated a weak though opposite correlation with CBF (r = 0.0942, p = 0.2733). The present data emphasize the clinical significance of monitoring of cerebral blood flow and metabolism in TBI and provide evidence for metabolic coupling between astrocytes and neurons.

Adult↗

PubMed2005

Posttraumatic vasospasm: the epidemiology, severity, and time course of an underestimated phenomenon: a prospective study performed in 299 patients.

OBJECT: The purpose of this prospective study was to evaluate the cumulative incidence, duration, and time course of cerebral vasospasm after traumatic brain injury (TBI) in a cohort of 299 patients. METHODS: Transcranial Doppler (TCD) ultrasonography studies of blood flow velocity in the middle cerebral and basilar arteries (VMCA and VBA, respectively) were performed at regular intervals during the first 2 weeks posttrauma in association with 133Xe cerebral blood flow (CBF) measurements. According to current definitions of vasospasm, five different criteria were used to classify the patients: A (VMCA > 120 cm/second); B (VMCA > 120 cm/second and a Lindegaard ratio [LR] > 3); C (spasm index [SI] in the anterior circulation > 3.4); D (VBA > 90 cm/second); and E (SI in the posterior circulation > 2.5). Criteria C and E were considered to represent hemodynamically significant vasospasm. Mixed-effects spline models were used to analyze the data of multiple measurements with an inconsistent sampling rate. Overall 45.2% of the patients demonstrated at least one criterion for vasospasm. The patients in whom vasospasm developed were significantly younger and had lower Glasgow Coma Scale scores on admission. The normalized cumulative incidences were 36.9 and 36.2% for patients with Criteria A and B, respectively. Hemodynamically significant vasospasm in the anterior circulation (Criterion C) was found in 44.6% of the patients, whereas vasospasm in the BA-Criterion D or E-was found in only 19 and 22.5% of the patients, respectively. The most common day of onset for Criteria A, B, D, and E was postinjury Day 2. The highest risk of developing hemodynamically significant vasospasm in the anterior circulation was found on Day 3. The daily prevalence of vasospasm in patients in the intensive care unit was 30% from postinjury Day 2 to Day 13. Vasospasm resolved after a duration of 5 days in 50% of the patients with Criterion A or B and after a period of 3.5 days in 50% of those patients with Criterion D or E. Hemodynamically significant vasospasm in the anterior circulation resolved after 2.5 days in 50% of the patients. The time course of that vasospasm was primarily determined by a decrease in CBF. CONCLUSIONS: The incidence of vasospasm after TBI is similar to that following aneurysmal subarachnoid hemorrhage. Because vasospasm is a significant event in a high proportion of patients after severe head injury, close TCD and CBF monitoring is recommended for the treatment of such patients.

Adult↗

PubMed2004

Selective metabolic reduction in gray matter acutely following human traumatic brain injury.

The aim of this study was to determine whether the apparent loss of overall gray-white matter contrast (GM/WM) seen on FDG-PET imaging reflects the differential changes of glucose metabolic rate (CMRglc) in cortical gray mater (GM) and subcortical white mater (WM) following TBI. The clinical significance of the CMRglc GM-to-WM ratio was also evaluated. Nineteen normal volunteers and 14 TBI patients were studied. Each subject had a quantitative FDG-PET, a quantitative H215O-PET and a MR scan acutely following TBI. Stabilities of the global and regional FDG lumped constants (LC) were studied. Parametric images (pixel unit: mg/min/100g) of FDG uptake rate (CURFDG) and CMRglc were generated. The changes of CMR(glc) in whole brain, GM and WM were studied separately by using a MRI-segmentation-based technique. The GM-to-WM ratios of both CURFDG and CMRglc images were significantly (p < 0.001) decreased (>31%) in TBI patients. The global LC value reduced significantly (p < 0.01) in TBI patients. The CMRglc decreased significantly (p < 0.001) in GM but not in WM (p > 0.1). Kinetic analysis revealed significant (p < 0.001) decrease of GM hexokinase activity in TBI patients. The GM-to-WM ratios of CMRglc correlated (r = 0.64) with the initial Glasgow Coma Score (GCS) of TBI patients. The patients with higher CMRglc GM-to-WM ratios (>1.54) showed good recovery 12 months after TBI. There was a selective CMRglc reduction in cortical GM following TBI. The pathophysiological basis for the reduction in GM-to-WM CMRglc ratio seen on FDG-PET imaging following TBI remains to be determined.

Acute Disease↗

PubMed2004

Subcortical white matter metabolic changes remote from focal hemorrhagic lesions suggest diffuse injury after human traumatic brain injury.

OBJECTIVE: We used positron emission tomographic studies to prospectively examine the relationship between glucose and oxidative metabolism in the subcortical white matter (WM) acutely after traumatic brain injury (TBI). The objective was to determine the nature, extent, and degree of metabolic abnormalities in subcortical brain regions remote from hemorrhagic lesions. METHODS: Sixteen normal volunteers and 10 TBI patients (Glasgow Coma Scale score, 4-10; age, 17-64 yr; 6 with focal and 4 with diffuse injury) were studied. Each subject underwent dynamic positron emission tomographic studies using [(15)O]CO, (15)O(2), [(15)O]H(2)O, and fluorodeoxyglucose plus a magnetic resonance imaging scan acutely after TBI. Parametric images of the metabolic rate of oxygen and metabolic rate of glucose were generated, and a molar oxygen-to-glucose utilization ratio was calculated. Data from gray matter and WM remote from hemorrhagic lesions, plus whole brain, were analyzed. RESULTS: There was a significant reduction in the subcortical WM oxygen-to-glucose utilization ratio after TBI compared with normal values (3.99 +/- 0.77 versus 5.37 +/- 1.00; P < 0.01), whereas the mean cortical gray matter and whole-brain values remained unchanged. WM metabolic changes, which were diffuse throughout the hemispheres, were characterized by a reduction in the metabolic rate of oxygen without a concomitant drop in the metabolic rate of glucose. CONCLUSION: The extent and degree of subcortical WM metabolic abnormalities after moderate and severe TBI suggest that diffuse WM injury is a general phenomenon after such injuries. This pervasive finding may indicate that the concept of focal traumatic injury, although valid from a computed tomographic imaging standpoint, may be misleading when considering metabolic derangements associated with TBI.

Adolescent↗

PubMed2004

Accuracy of a method using short inhalation of (15)O-O(2) for measuring cerebral oxygen extraction fraction with PET in healthy humans.

UNLABELLED: PET with short inhalation of (15)O-O(2) provides regional oxygen extraction fraction (OEF) in a shorter acquisition time and with less radiation exposure than does the steady-state method. The purpose of this study was to test the accuracy of the short-inhalation technique for estimating OEF in healthy human volunteers. METHODS: The final study population included 16 healthy volunteers, who underwent a series of dynamic PET scans consisting of short inhalation of (15)O-CO, short inhalation of (15)O-O(2), and a bolus infusion of (15)O-H(2)O to generate parametric images for cerebral blood volume (CBV), cerebral blood flow (CBF), OEF, and metabolic rate of oxygen (CMRO(2)). About 45 min before PET emission scanning, arterial and jugular blood was sampled through a catheter inserted in a radial artery and the right jugular bulb, respectively. PET-derived OEF (OEFpet) of the whole brain was compared with OEF calculated from the arteriovenous blood-sampling technique (OEFav). RESULTS: Whole-brain-averaged CBF (mean +/- SD) measured with PET was 0.40 +/- 0.06 (range, 0.30-0.55) mL/g/min, CBV was 0.05 +/- 0.01 (range, 0.04-0.09) mL/g, CMRO(2) was 2.85 +/- 0.39 (range, 2.35-3.84) mL/100 g/min, and OEFpet was 0.39 +/- 0.06 (range, 0.30-0.51). OEFpet showed a slightly higher value than did OEFav (0.36 +/- 0.05 [range, 0.29-0.46]), but the difference was not significant. The difference in the 2 measurements (OEFpet - OEFav) did not correlate with CBF (r = -0.16; P = not statistically significant [NS]), CBV (r = -0.20; P = NS), CMRO(2) (r = -0.16; P = NS), partial arterial oxygen pressure (r = 0.29; P = NS) or partial arterial carbon dioxide pressure (r = -0.17; P = NS). CONCLUSION: Compared with the arteriovenous blood-sampling technique, a technique using short inhalation of (15)O-O(2) did not significantly over- or underestimate global OEF in healthy human volunteers. The PET technique reasonably estimated the cerebral OEF in local brain tissues of healthy human volunteers.

Adult↗

PubMed2004

Acute changes in regional cerebral (18)F-FDG kinetics in patients with traumatic brain injury.

UNLABELLED: During the acute phase after traumatic brain injury (TBI), the metabolic state is regionally heterogeneous. The purpose of this study was to characterize contusional, pericontusional, and remote regions of TBI by estimating glucose transporter and hexokinase activities on the basis of (18)F-FDG kinetic modeling. METHODS: A standard 2-compartment model was used to measure (18)F-FDG kinetic parameters in 21 TBI patients with cerebral contusions studied during the acute phase (3.1 +/- 2.1 [mean +/- SD] d after injury). Nineteen patients also underwent (15)O-water PET to measure regional cerebral blood flow (CBF). A control study ((18)F-FDG and (15)O-water) was done with 18 healthy volunteers. The rate constants K(i), K(1), and k(3) were assumed to represent the uptake, transport, and hexokinase activity of (18)F-FDG, respectively; K(i) was calculated as K(1) x [k(3)/(k(2) + k(3))]. RESULTS: The areas of contusional and pericontusional tissues located 4.5, 13.5, and 22.5 mm away from the contusion (PC(4.5), PC(13.5), and PC(22.5), respectively) demonstrated significantly reduced K(1) values, whereas the K(1) values for remote areas remained normal. The k(3) values were significantly reduced regardless of the distance from the contusion. Pericontusional areas with CT- or MRI-evidenced tissue damage showed significantly lower K(i) (P < 0.001), CBF (P < 0.01), and K(1) (P < 0.0001) values than did areas without such damage, whereas the k(3) values did not differ significantly. Seven patients showed regionally increased (18)F-FDG uptake (hot spots) in pericontusional areas. The k(3) value for the hot spots (0.086 +/- 0.024/min) was significantly higher than that for the remote cortex (P < 0.01), whereas the K(i), CBF, and K(1) values did not show significant differences. Patients with hot spots showed significantly higher K(i) and k(3) values in PC(4.5) (P < 0.05) and higher k(3) values in PC(22.5) (P < 0.05) than did patients without hot spots, whereas the K(1) and CBF values did not differ significantly. CONCLUSION: Brain tissue (18)F-FDG kinetics in TBI patients were consistent with reduced hexokinase activity in the whole brain (including apparently uninjured cortex), whereas glucose transport was impaired only in the area immediately around the contusion. Pericontusional high levels of (18)F-FDG uptake observed in a subgroup of patients could have been the result of regionally increased hexokinase activity.

Acute Disease↗

PubMed2003

Energy dysfunction as a predictor of outcome after moderate or severe head injury: indices of oxygen, glucose, and lactate metabolism.

UNLABELLED: The purpose of this study was to determine if the relationship between abnormalities in glucose, lactate, and oxygen metabolism were predictive of neurologic outcome after moderate or severe head injury, relative to other known prognostic factors. Serial assessments of the cerebral metabolic rates for glucose, lactate, and oxygen were performed using a modified Kety-Schmidt method. In total, 31 normal control subjects were studied once, and 49 TBI patients (mean age 36+/-16 years, median GCS 7) were studied five times median per patient from postinjury days 0 to 9. Univariate and multivariate analyses were performed. Univariate analysis showed that the 6-month postinjury Glasgow Outcome Scale (GOS) was most strongly associated with the mean cerebral metabolic rate of oxygen (CMRO2) (P = 0.0001), mean arterial lactate level (P = 0.0001), mean arterial glucose (P = 0.0008), mean cerebral blood flow (CBF), (P = 0.002), postresuscitation GCS (P = 0.003), and pupillary status (P = 0.004). Brain lactate uptake was observed in 44% of all metabolic studies, and 76% of patients had at least one episode of brain lactate uptake. By dichotomized GOS, patients achieving a favorable outcome (GOS 4-5) were distinguished from those with an unfavorable outcome (GOS1-3) by having a higher CMRO2 (P = 0.003), a higher rate of abnormal brain lactate uptake relative to arterial lactate levels (P = 0.04), and lesser degrees of blood-brain barrier damage based on CT findings (P = 0.03). CONCLUSIONS: During the first 6 days after moderate or severe TBI, CMRO2 and arterial lactate levels are the strongest predictors of neurologic outcome. However, the frequent occurrence of abnormal brain lactate uptake despite only moderate elevations in arterial lactate levels in the favorable outcome patients suggests the brain's ability to use lactate as a fuel may be another key outcome predictor. Future studies are needed to determine to what degree nonglycolytic energy production from alternative fuels such as lactate occurs after TBI and whether alternative fuel administration is a viable therapy for TBI patients.

Adult↗

PubMed2003

Correlation of regional metabolic rates of glucose with glasgow coma scale after traumatic brain injury.

UNLABELLED: After traumatic brain injury (TBI), subcortical white matter damage may induce a functional disconnection leading to a dissociation of regional cerebral metabolic rate of glucose (CMRglc) between the cerebral cortex and deeper brain regions. Therefore, thalamic and brain stem CMRglc may have a closer correlation than does the cerebral cortex with depth of coma after TBI. METHODS: Eleven adult healthy volunteers and 23 adult patients with TBI (median initial Glasgow Coma Scale score [GCSini], 8) underwent (18)F-FDG PET within 5 d after injury. The CMRglc of cortical areas (remote from hemorrhagic lesions), striatum, thalamus, brain stem, cerebellar cortex, and whole brain was compared with severity of injury and the level of consciousness evaluated using GCSini and the Glasgow Coma Scale score at the time of PET (GCSpet). RESULTS: The regional CMRglc of the brain stem is relatively unaffected by the TBI. Compared with healthy volunteers, TBI patients exhibited significantly depressed CMRglc in the striatum (3.9 +/- 1.3 vs. 5.1 +/- 0.9 mg/100 g/min, P < 0.05) and thalamus (3.1 +/- 1.0 vs. 4.3 +/- 0.9 mg/100 g/min, P < 0.05). CMRglc levels were not statistically lower in the cerebellum (2.9 +/- 0.8 vs. 3.5 +/- 0.8 mg/100 g/min, P = NS) and brain stem (2.5 +/- 0.5 vs. 2.6 +/- 0.5 mg/100 g/min, P = NS). However, compared between comatose and noncomatose patients, CMRglc values in the thalamus (2.7 +/- 0.7 vs. 3.6 +/- 1.2 mg/100 g/min, P < 0.05), brain stem (2.2 +/- 0.4 vs. 2.8 +/- 0.5 mg/100 g/min, P < 0.01), and cerebellar cortex (2.6 +/- 0.5 vs. 3.4 +/- 1.0 mg/100 g/min, P < 0.05) were significantly lower in comatose patients. When individual values of regional CMRglc were plotted against posttraumatic level of consciousness, CMRglc values for the thalamus, brain stem, and cerebellum significantly correlated with the level of consciousness at the time of PET (r = 0.58, P < 0.01; r = 0.66, P < 0.01; r = 0.64, P < 0.01, respectively). CT or MRI findings were normal for the analyzed structures except for 3 patients with diffuse axonal injury of the brain stem. The presence of shear injury was associated with poor GCSini (P < 0.05.) but was not related to GCSpet and brain stem CMRglc. CONCLUSION: A PET investigation using (18)F FDG demonstrated a significant difference in glucose metabolism in the thalamus, brain stem, and cerebellum between comatose and noncomatose patients acutely after TBI. The metabolic rate of glucose in these regions significantly correlated with the level of consciousness at the time of PET.

Adolescent↗

PubMed2002

Subarachnoid hemorrhage induces dynamic changes in regional cerebral metabolism in rats.

Following a subarachnoid hemorrhage (SAH), adult rats exhibit dynamic regional changes in cerebral glucose metabolism characterized by an increase in metabolic rates and a subsequent upregulation of cytochrome oxidase (CO). We evaluated both local cerebral metabolic rates for glucose (ICMRglc: (mol/100 g/min) and CO in 23 brain regions of interest (ROI). Sham animals underwent anesthesia and superficial surgery; saline-controls received an injection of 0.9% saline into the cisterna magna; and SAH rats received an injection of autologous blood into the cisterna magna. This blood, measured by albumin labeled with radioactive carbon 14, distributed throughout the brain but predominated ventrally. After experimental animals were sacrificed at day 0 (3 h), 1, 3, and 7 days postinjection, ROI were analyzed using [14C]2-deoxy-D-glucose autoradiography and CO histochemistry. ICMRglc in SAH rats increased in many regions (ranging from 0.7% to 32.2% above sham levels). Cytochrome oxidase also increased from 1% to 9% above sham levels, peaking on day 3. Conversely, saline-controls exhibited prolonged depression of ICMRglc (ranging from 11% to 35% below sham levels) and CO (ranging from 4% to 11% below sham levels) from day 0 through day 7. All saline-control ROI for all time points showed this metabolic depression, and between 91% and 95% of saline-control ROI presented lower CO levels as compared to sham. Overall, ICMRglc and CO levels were greater in SAH than in saline-control ROI. However, when considering the influence of subarachnoid blood on metabolic changes in SAH animals, both CO and 2DG levels did not correlate well with the amount of 14C-albumin binding. While previous studies have measured both metabolic rates of glucose and CO soon after SAH, this is the first to simultaneously conduct these measurements in the same SAH rat model.

Animals↗

PubMed2002

Multimodal quantitation of the effects of endovascular therapy for vasospasm on cerebral blood flow, transcranial doppler ultrasonographic velocities, and cerebral artery diameters.

OBJECTIVE: The goal of this study was to quantify the effects of endovascular therapy on vasospastic cerebral vessels. METHODS: We reviewed the medical records for 387 patients with ruptured intracranial aneurysms who were treated at a single institution (University of California, Los Angeles) between May 1, 1993, and March 31, 2001. Patients who developed cerebral vasospasm and underwent cerebral arteriographic, transcranial Doppler ultrasonographic, and cerebral blood flow (CBF) studies before and after endovascular therapy for cerebral arterial spasm (vasospasm) were included in this study. RESULTS: Forty-five patients fulfilled the aforementioned criteria and were treated with either papaverine infusion, papaverine infusion with angioplasty, or angioplasty alone. After balloon angioplasty (12 patients), CBF increased from 27.8 +/- 2.8 ml/100 g/min to 28.4 +/- 3.0 ml/100 g/min (P = 0.87); the middle cerebral artery blood flow velocity was 1 57.6 +/- 9.4 cm/s and decreased to 76.3 +/- 9.3 cm/s (P < 0.05), with a mean increase in cerebral artery diameters of 24.4%. Papaverine infusion (20 patients) transiently increased the CBF from 27.5 +/- 2.1 ml/100 g/min to 38.7 +/- 2.8 ml/100 g/min (P < 0.05) and decreased the middle cerebral artery blood flow velocity from 109.9 +/- 9.1 cm/s to 82.8 +/- 8.6 cm/s (P < 0.05). There was a mean increase in vessel diameters of 30.1% after papaverine infusion. Combined treatment (13 patients) significantly increased the CBF from 33.3 +/- 3.2 ml/100 g/min to 41.7 +/- 2.8 ml/100 g/min (P< 0.05) and decreased the transcranial Doppler velocities from 148.9 +/- 12.7 cm/s to 111.4 +/- 10.6 cm/s (P < 0.05), with a mean increase in vessel diameters of 42.2%. CONCLUSION: Balloon angioplasty increased proximal vessel diameters, whereas papaverine treatment effectively dilated distal cerebral vessels. In our small series, we observed no correlation between early clinical improvement or clinical outcomes and any of our quantitative or physiological data (CBF, transcranial Doppler velocities, or vessel diameters).

Adult↗

PubMed2002

Progressive hemorrhage after head trauma: predictors and consequences of the evolving injury.

OBJECT: Progressive intracranial hemorrhage after head injury is often observed on serial computerized tomography (CT) scans but its significance is uncertain. In this study, patients in whom two CT scans were obtained within 24 hours of injury were analyzed to determine the incidence, risk factors, and clinical significance of progressive hemorrhagic injury (PHI). METHODS: The diagnosis of PHI was determined by comparing the first and second CT scans and was categorized as epidural hematoma (EDH), subdural hematoma (SDH), intraparenchymal contusion or hematoma (IPCH), or subarachnoid hemorrhage (SAH). Potential risk factors, the daily mean intracranial pressure (ICP), and cerebral perfusion pressure were analyzed. In a cohort of 142 patients (mean age 34 +/- 14 years; median Glasgow Coma Scale score of 8, range 3-15; male/female ratio 4.3: 1), the mean time from injury to first CT scan was 2 +/- 1.6 hours and between first and second CT scans was 6.9 +/- 3.6 hours. A PHI was found in 42.3% of patients overall and in 48.6% of patients who underwent scanning within 2 hours of injury. Of the 60 patients with PHI, 87% underwent their first CT scan within 2 hours of injury and in only one with PHI was the first CT scan obtained more than 6 hours postinjury. The likelihood of PHI for a given lesion was 51% for IPCH, 22% for EDH, 17% for SAH, and 11% for SDH. Of the 46 patients who underwent craniotomy for hematoma evacuation, 24% did so after the second CT scan because of findings of PHI. Logistic regression was used to identify male sex (p = 0.01), older age (p = 0.01), time from injury to first CT scan (p = 0.02), and initial partial thromboplastin time (PTT) (p = 0.02) as the best predictors of PHI. The percentage of patients with mean daily ICP greater than 20 mm Hg was higher in those with PHI compared with those without PHI. The 6-month postinjury outcome was similar in the two patient groups. CONCLUSIONS: Early progressive hemorrhage occurs in almost 50% of head-injured patients who undergo CT scanning within 2 hours of injury, it occurs most frequently in cerebral contusions, and it is associated with ICP elevations. Male sex, older age, time from injury to first CT scan, and PTT appear to be key determinants of PHI. Early repeated CT scanning is indicated in patients with nonsurgically treated hemorrhage revealed on the first CT scan.

Adolescent↗

PubMed2002

Early and persistent impaired percent alpha variability on continuous electroencephalography monitoring as predictive of poor outcome after traumatic brain injury.

OBJECT: Early prediction of outcomes in patients after they suffer traumatic brain injury (TBI) is often nonspecific and based on initial imaging and clinical findings alone, without direct physiological testing. Improved outcome prediction is desirable for ethical, social, and financial reasons. The goal of this study was to determine the usefulness of continuous electroencephalography (EEG) monitoring in determining prognosis early after TBI, while the patient is in the intensive care unit. METHODS: The authors hypothesized that the reduced percentage of alpha variability (PAV) in continuous EEG tracings indicates a poor prognosis. Prospective continuous EEG monitoring was performed in 89 consecutive patients with moderate to severe TBI (Glasgow Coma Scale [GCS] Scores 3-12) from 0 to 10 days after injury. The PAV was calculated daily, and the time course and trends of the PAV were analyzed in comparison with the patient's Glasgow Outcome Scale (GOS) score at the time of discharge. In patients with GCS scores of 8 or lower, a PAV value of 0.1 or lower is highly predictive of a poor outcome or death (positive predictive value 86%). The determinant PAV value was obtained by Day 3 after injury. Persistent PAV values of 0.1 or lower over several days or worsening of the PAV to a value of 0.1 or lower indicated a high likelihood of poor outcome (GOS Scores 1 and 2). In comparison with the combination of traditional initial clinical indicators of outcome (GCS score, pupillary response to light, patient age, results of computerized tomography scanning, and early hypotension or hypoxemia), the early PAV value during the initial 3 days after injury independently improved prognostic ability (p < 0.01). CONCLUSIONS: Continuous EEG monitoring performed with particular attention paid to the PAV is a sensitive and specific method of prognosis that can indicate outcomes in patients with moderate to severe TBI within 3 days postinjury.

Adult↗

PubMed2002

Efficacy of hyperventilation, blood pressure elevation, and metabolic suppression therapy in controlling intracranial pressure after head injury.

OBJECT: Hyperventilation therapy, blood pressure augmentation, and metabolic suppression therapy are often used to reduce intracranial pressure (ICP) and improve cerebral perfusion pressure (CPP) in intubated head-injured patients. In this study, as part of routine vasoreactivity testing, these three therapies were assessed in their effectiveness in reducing ICP. METHODS: Thirty-three patients with a mean age of 33 +/- 13 years and a median Glasgow Coma Scale (GCS) score of 7 underwent a total of 70 vasoreactivity testing sessions from postinjury Days 0 to 13. After an initial 133Xe cerebral blood flow (CBF) assessment, transcranial Doppler ultrasonography recordings of the middle cerebral arteries were obtained to assess blood flow velocity changes resulting from transient hyperventilation (57 studies in 27 patients), phenylephrine-induced hypertension (55 studies in 26 patients), and propofol-induced metabolic suppression (43 studies in 21 patients). Changes in ICP, mean arterial blood pressure (MABP), CPP, PaCO2, and jugular venous oxygen saturation (SjvO2) were recorded. With hyperventilation therapy, patients experienced a mean decrease in PaCO2 from 35 +/- 5 to 27 +/- 5 mm Hg and in ICP from 20 +/- 11 to 13 +/- 8 mm Hg (p < 0.001). In no patient who underwent hyperventilation therapy did SjvO2 fall below 55%. With induced hypertension, MABP in patients increased by 14 +/- 5 mm Hg and ICP increased from 16 +/- 9 to 19 +/- 9 mm Hg (p = 0.001). With the aid of metabolic suppression, MABP remained stable and ICP decreased from 20 +/- 10 to 16 +/- 11 mm Hg (p < 0.001). A decrease in ICP of more than 20% below the baseline value was observed in 77.2, 5.5, and 48.8% of hyperventilation, induced-hypertension, and metabolic suppression tests, respectively (p < 0.001 for all comparisons). Predictors of an effective reduction in ICP included a high PaCO2 for hyperventilation, a high study GCS score for induced hypertension, and a high PaCO2 and a high CBF for metabolic suppression. CONCLUSIONS: Of the three modalities tested to reduce ICP, hyperventilation therapy was the most consistently effective, metabolic suppression therapy was variably effective, and induced hypertension was generally ineffective and in some instances significantly raised ICP. The results of this study suggest that hyperventilation may be used more aggressively to control ICP in head-injured patients, provided it is performed in conjunction with monitoring of SjvO2.

Adult↗